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Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Activation of PPARγ by a Natural Flavonoid Modulator, Apigenin Ameliorates Obesity-Related Inflammation Via
Xiujing Feng1, Dan Weng2, Feifei Zhou1
1State Key Laboratory of Pharmaceutical Biotechnology, School of life Sciences, Nanjing University, Nanjing 210046, China.
Abstract:
PPARγ has emerged as a master regulator of macrophage polarization and is the molecular target of the thiazolidinedione drugs. Here we show that apigenin binds and activates PPARγ by acting as a modulator. Activation of PPARγ by apigenin blocks p65 translocation into nuclei through inhibition of p65/PPARγ complex translocation into nuclei, thereby decreasing NF-κB activation and favoringM2 macrophage polarization. In HFD and ob/ob mice, apigenin significantly reverses M1 macrophage into M2 and reduces the infiltration of inflammatory cells in liver and adipose tissues, as well as decreases the levels of pro-inflammatory cytokines, thereby alleviating inflammation. Strikingly, apigenin reduces liver and muscular steatosis, decreases the levels of ALT, AST, TC and TG, improving glucose resistance obviously. Unlike rosiglitazone, apigenin does not cause significant weight gain, osteoporosis et al. Our findings identify apigenin as a modulator of PPARγ and a potential lead compound for treatment of metabolic disorders.
Insights
Apigenin activates PPARγ, modulating macrophage polarization and reducing inflammation. This natural compound alleviates metabolic disorders like fatty liver and insulin resistance without adverse effects, unlike some drugs.
Area of Science:
- Biochemistry
- Immunology
- Metabolic Disorders
Background:
- Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of macrophage polarization and a target for thiazolidinedione drugs.
- Understanding natural compounds that modulate PPARγ offers potential therapeutic strategies for metabolic diseases.
Purpose of the Study:
- To investigate apigenin's role as a modulator of PPARγ.
- To evaluate apigenin's effects on macrophage polarization and inflammatory responses.
- To assess apigenin's efficacy in treating diet-induced and genetic metabolic disorders.
Main Methods:
- In vitro assays to confirm apigenin binding and activation of PPARγ.
- Studies on macrophage polarization (M1 vs. M2) influenced by apigenin.
- In vivo experiments using high-fat diet (HFD) and ob/ob mice models.
- Analysis of inflammatory markers, liver/muscle steatosis, and glucose metabolism.
Main Results:
- Apigenin binds and activates PPARγ, inhibiting NF-κB activation and promoting M2 macrophage polarization.
- Apigenin treatment reversed M1 to M2 polarization, reduced inflammatory cell infiltration, and lowered pro-inflammatory cytokines in HFD and ob/ob mice.
- Apigenin significantly reduced liver and muscle steatosis, improved lipid profiles (ALT, AST, TC, TG), and enhanced glucose resistance.
- Apigenin did not induce weight gain or osteoporosis, unlike rosiglitazone.
Conclusions:
- Apigenin acts as a PPARγ modulator, offering a novel mechanism for controlling inflammation and metabolic dysfunction.
- Apigenin demonstrates therapeutic potential for metabolic disorders, including fatty liver and insulin resistance, with a favorable safety profile.
- Apigenin represents a promising lead compound for developing new treatments for metabolic diseases.
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